Zika fever is caused by a flavivirus, a single stranded positive RNA virus, that belongs to the Flaviviridae family. The Zika virus (ZIKV) was recently introduced in Brazil and has been associated with an expressive increase in the number of infants with microcephaly born to mothers who are believed to be infected. The viruses of this family are usually transmitted by bites of mosquitoes of the Aedes aegypti mosquito, and can cause from mild infections with fever-like fever to severe clinical manifestations such as hemorrhages and encephalitis. The high identity in the amino acid sequence (approximately 55%) between ZIKV and different serotypes of dengue virus (DENV 1-4) may lead to cross-recognition of different proteins by the immune system, which may favor both protection and pathogenesis of these diseases. For example, cross-recognition of antibodies against the different serotypes of DENV may lead to a phenomenon known as "antibody dependent enhancement" (ADE) which predicts the potentiation of a secondary infection when the primary infection is caused by a different serotype virus. Therefore, it is quite relevant to study the humoral component of the response against ZIKV and to assess whether the antibodies induced during infection may have some cross-reactivity against DENV. Thus, this project aims to study in greater detail the humoral immune response induced in patients infected by ZIKV using an innovative approach that consists of the cloning and expression of monoclonal antibodies (mAbs) from the DNA sequences coding for the variable portion of the receptor-specific B cells for viral envelope protein obtained from patients with recent ZIKV infection.
News published in Agência FAPESP Newsletter about the scholarship: